Gait disorders

Gait Disorders by Sruthi Meenaxshi

1. Gait disorders - S.R.Sruthi Meenaxshi MODERATOR:DR.DHIRAJ KISHORE

2. Gait Defined as Bipedal, biphasic , forward propulsion of centre of gravity of the human body, in which there are alternate sinuous movements of different segments of body with least expenditure of energy. In humans two thirds of total body weight is centered in the upper body which makes for inherent instabilty .

3. The limits of stability have been defined as an inverted cone with the apex at the feet and base defining perimeter at the head . Sway outside of this perimeter results in instabilty . The dimensions of the base of the cone are roughly 12.5 degrees in anteroposterior diameter and 16 degrees laterally

4. Requirement for normal gait Antigravity support of the body Stepping Maintenance of equilibrium Propulsion

5. GAIT CYCLE A gait cycle consists of two steps or one stride ‘the activities that occur from the point of initial contact of one lower extremity to the point at which the same extremity contacts the ground again ‘ During one gait cycle, each extremity passes through two phases, a single stance phase and a single swing phase

6. Components of stance phase Stance phase comprises 60% of the gait cycle Heel strike – moment when the heel first strikes the ground Foot flat – from heel strike to when the full foot is in contact with the ground Midstance – body weight is directly over the stance leg Heel off – moment the heel of the stance leg leaves the ground Toe off – when only the toe of the stance leg is in contact with the ground

7. Components of the Swing Phase Swing phase comprises 40% of the gait cycle Acceleration – the toe of the stance leg leaves the ground and begins to swing forward Midswing – the swinging leg is directly beneath the body Deceleration – the swinging leg continues forward towards knee extension but is slowing down as it travels, stopping just prior to full knee extension and heel contact with the ground

8. SWING PHASE

9. Things to look for while observing gait Feet separation Stride length Foot drop Pelvic tilt Arm swing

10. ABNORMAL GAITS

11. Gait disturbances can arise from disorders of Frontal lobe lesions Sensory pathways (sensory ataxia ) Cerebellum Posterior column, dorsal root ganglia, peripheral nerves Extrapyramidal system Vestibular system

12. SENSORY ATAXIA Disturbances in the sensory input to the cerebellum The nervous system is deprived of sensory information primarily proprioception and joint position sense Romberg sign Loss of tendon reflexes Features of peripheral neuropathy WIDE BASED HIGH STEPPAGE GAIT

13. 26 year old female , presented with C/0 progressive tingling/ numbness, weakness, Ataxia with high steppage gait. On examination there was spastic parapersis with extensor plantar. Sensory examination revealed diminished touch, pressure, vibration and proprioception. Rombergs test was positive.

14. 8 year old male present ed with C/o Progressive ataxia , with weakness of limbs and frequent falls , visual impairment with incoordination.On examination patient had scoliosis , spasticity , plantar was extensor , knee and ankle reflexes were absent with foot deformity . Sensory examination revealed decreased proprioception and vibration.

15. FRIEDREICH ATAXIA - Autosomal Recessive -unstable expansion of GAA repeats  Frataxin protein iron accumulation in mitochondria  mitochondrial injury neuronal injury Dorsal root ganglion : absent reflexes Dorsal column degeneration : dec post col senses Spinocerebellar tract : gait ataxia , dysrthria Corticospinal tract – Babinski positive Associated cardiomyopathy (90%) Diabetes ( 10 %) , optic atrophy , spine and foot deformity

16. CAUSES OF SENSORY ATAXIA: Causes- subacute combined degeneration of the cord ( vit B12 deficiency ), diabetes sensory neuropathy tabes dorsalis , Friedreich ataxia, cervical spondylosis , meningioma

17. Cerebellar Ataxia Wide based gait, clumpsy , staggering, unsteady, lurching titubating The patient is unable to walk in a straight line , tandem walking is impaired With hemispheric lesion the patient will stagger and deviates towards the involved side With lesion of cerebellar vermis,the patient will exhibit a lurching, staggering gait, but without laterality Cerebellar ataxia is present with both eyes open and closed ( romberg negative)

18. Approach to patient with cerebellar ataxia

19. PROGRESSION Progessive Static Intermittent symptoms Reversible Ataxia

20. STATIC ATAXIAS : Vascular causes REVERSIBLE ATAXIA : infectious causes – post viral thyroid drugs / toxins INTERMITTENT ATAXIA Episodic Ataxia ( inherited Etiology )

21. FOCAL/SYMMETRIC ATAXIA Cerebellar symptoms on same side of lesionor bilateral symptoms FOCAL ATAXIAS: vascular causes , multiple sclerosis, cerebellar abscess, cerebellar glioma , PML , HIV, congenital causes SYMMETRICAL ATAXIA : -intoxication , nutritional, Post infectious,Hypothyroid , Autoimmune causes

22. ACQUIRED ATAXIA First rule out structural causes ( MRI/ CT HEAD ) CV J anomalies Posterior fossa tumours Demyelinating diseases Hypoxic encephalopathies Vascular causes – infarct, hemorhage

23. TOXINS Cancer chemotherapeutics -5 FU, Cytarabine Metals : bismuth , Mercury (Ataxia, paresthesia , restricted visual defects, LEAD ( anemia , ataxia, foot drop, wrist drop, basophilic stippling ) Solvents : paint thinner , toluene cognitive defects plus pyramidal tract signs ) Anticonvulsants – phenytoin ( purkinje cell loss )avoid in epileptics with ataxia

24. Infections VZV HSV EBV Bickerstaffs encephalitis (brain stem : post infectious / external ophthalmoplegia /lower limb areflexia , extensor plantar, ataxia , drowsiness HIV ( lymphoma , PML, Toxoplasmosis ) CJD ( 17 % classic CJD , Ataxic variant of CJD) Syphilis Whipple diseas e

25. 54 year old male recently diagnosed diabetic and hypertensive came with complaints of acute onset d he noticed progressively He gradually developed progressive truncal ataxia with ataxic dysarthria and intentional tremor, rapidly worsening over a period of 2 weeks .on examination . Prominent ataxic dysarthria , dysmetria of upper limbs more than lower limb, dysdiadochokinesia and intentional tremors were observed . No cranial neuropathy . Upper and lower limb power was 5/5, with brisk tendon reflexes, hypotonia in the upper limbs and mild spasticity in the lower limbs.No chronic medication intake. On MRI inital3 weeks of illness was normal. All hematological and biochemical parameters were within normal limits.   ANA, Anti DSDNA, APLA, Canca , Panca , CSF analysis were within normal. CSF electrophoresis was negative for oligoclonal bands and malignant cells. CSF Cr Ag, PCR-TB, HSV I and II and arbovirus were negative. A 4cm lympnode was palpable over the axilla . Lymphnode biopsy revealed hogkins lymphoma . Anti TR anti body was performed was found to be positive. Mr i was repeated showed hyperintensites in bilateral cerebellar hemisphere. Patient was treated with 6 cycles of chemotherapy. Treatment options are limited and are largely dependent on treating the underlying malignancy to lower antibody titers . Other therapeutic interventions such as intravenous immunoglobulins , plasmapheresis and immunosuppressive therapy

26. Case of acute paraneoplastic pancerebellitis

27. AUTOIMMUNE CAUSES Paraneoplastic Syndromes Anti HU abs – small cell cancer lung ( extrapyramidal signs) Anti YO Abs – ovarian cancer Anti Ri abs – breast cancer Anti Tr Antibody – hodgkins lymphoma

28. 60 year old man presented with incoordination of movements with tremor , with wide based staggering gait , nystagmus and scanning speech. He gives a history than his 32 year old son has similar complaints . On examination power is normal, Tone is spastic,knee and ankle reflex was absent plantar was extensor. Dymmetria , dysdiadakinesis , pendular knee jerk was present. MRI showed diffuse cerebellar atrophy

29. Spinocerebellar Ataxia Autosomal dominant SCA 1-36 types , SCA1,2,3,7,17 due to CAG triplet repeat expansion codes for glutamine Protiens termed as ATAXINS- more than -40 glutamines potentially toxic for the neurons – leads to neuronal loss and gliosis SCA 8- CTG repeat,SCA 10 forms pentanucleotide repeats Anticipation ( earlier age on onset and aggressive course in successive generation )

30. SCA 1 middle life progressive cerebellar ataxia ,scanning sppech , nystagmus , dysarthria mild spascity , parkinsonian tremor , knee and ankle reflexes are lost. Extensor plantar response. Urinary and Fecal incontinence. Variable loss of purkinje cells. Gross atrophy of cerebellum SCA2- onset 2-65 years , ataxia , dysarthria , parkinsonian rigidity, optic atrophy and retinal degeneration Most common in India

31. MachadoJoseph disease (SCA3) Type 1 ( amyotrophic lateral sclerosis-parkinsonism- dystonic type) Weakness , spasticity, broad based lurching gait, ankle and patellar clonus . Extensor plantar.ophthalmoparesis and ocular prominence is early manifestion . There is no truncal titubation Prominence of horizontal and vertical nystagmus Loss of fast saccadic movements of eye Facial fasciculation,facial myokymia , lingual fasciculation without atrophy

32. Type 2 MC ( ataxia type ) 2 nd and 3 rd decade with corticospinal and extrapyramidal symptoms Dysarthria,cerebellar defects,opthalomoparesis , facial myokymia , facial fasciculation , spasticty is present Type 3 MJD ( Ataxia- Amyotrophic type ) Mean age on onset 25 years Pancerbellar ( dysarthria / gait distubance ) Distal sensory loss with features of peripheral neuropathy (loss of deep tendon reflexes ) No extrapyramidal or corticospinal involvement

33. SCA 6: Late onset AD ataxia Loss of vibration and proprioception Familial hemiplegic migraine Cerebellar atrophy SCA7: Presence of retinal pigment degeneration

34. 55 year old male hypertensive and Diabetic came with C/O weakness of right upperlimb and lowerlimb . On examination BP was 240/110 mm hg there was hypertonia , spasticity , plantar on right was extensor and left was flexor. CT head was revealed hemorrhage involving the internal capsule. GAIT ? Circumduction / Spastic gait

35. Spastic gait Spastic gait/ hemiparetic gait is caused by lesion interrupting the corticospinal pathway. Usually arms are flexed,adducted and internally rotated and legs extended. Patient drags the foot and scrapes the toes.

36. Spastic-ataxic gait Features of both spasticity and ataxia,it usually results in a spastic-ataxic gait. ‘ jiggling ’ or ‘ bobing ’ with tremulous,bouncing up and down body movements. Causes-vit-B12 deficiency, multiple sclerosis, HTLV/TSP, HIV associated vacuolar myelopathy , Copper deficiency

37. Parkinsonian gait The gait is slow,stiff and shuffling.as if patient is trying to catch his own centre of gravity Usually patient is stooped, with head and neck forward and knee flexed;the upper extrimities are flexed at the shoulders elbow and wrist. Cog wheel rigidity Arm swing is decreased

38. 60 year old male presented with gait disturbance in the short shuffling festinant gait , bradykinesia , pillrolling tremors with rigidity . Patient was diagnosed with parkinsons was started on levodopa with no benefit .six months later he c/o about gait disturbance with a feeling of right leg dragging with postural imbalance , and difficulties in swallowing and articulation.Toxic screen , gene testing for SCA was negative. Patient cognitive function gradually detetoriated.MRI revealed atrophy of cerebellum, pons and middle cerebellar peduncle .( Positron emission tomography (PET) was performed using  18 F-fluorodeoxyglucose (FDG), and showed decreased cerebral glucose metabolism on the bilateral basal ganglia, cerebellum, both parietal lobes, and left posterior cingulate gyrus .

39. Multisystem atropy

40. Multisystem atrophy Sporadic neurodegenerative disorder Pathology : cell loss , gliosis , glial cytoplasmic inclusions( alpha synnuclein ) in several CNS structures Mutation of COQ2 gene Affects both men and women Main features : autonomic failure ,parkinsonism(80 % MSA P), cerebellar ataxia (MSA c type)

41. Consensus statement for clinical diagnosis of MSA Autonomic and urinary dysfuntion 1)Orthostatic hypotension (reduction in atleast 30 mmhg systolic bp or atleast 15 mm hg of reduction of diastolic pressure after 3min of standing ) 2) Urinary incontinence ( persistant , involuntary partial or total bladder emptying , accompanied by erectile dysfunction or both )

42. MSA P associated Parkinsonism : Progressive akinesia and rigidity Jerky postural tremor and resting tremor Orofacial or craniocervical dystonia associated with high pitched dysarthria Postural instability early in disease with frequent falls

43. MSA – C: Gait ataxia Limb kinetic ataxia Scanning dysarthria Cerbellar and oculomotor disturbances

44. Disease progression Parkinsonism poorly responds to levodopa Cerebellar ataxia Early instablity and falls occur within 3 years of disease onset Rapid progression of the disease ( wheelchair bound despite dopaminergic treatment within 5 years of disease onset )

45. 60 year old male presented with H/o asymmetrical onset involuntary jerky movements, bradykinesia , forgetfulness, difficulty in swallowing, articulation.On examination muscle bulk was normal with no fasciculation . Tone of all limbs were increased (R>L) with marked axial rigidity .Reflexes were brisk with Right sided plantar flexor and left equivocal.sensory examination was normal. Patient had a stooped posture with short shuffling gait. Patient was started on levodopa but with no benefit . Patient developed repetitive contraction of muscle with feeling of arm and legs disconnected body.MRI was done revealed atrophy of fronto temporal region.

46. Case of corticobasal degeneration

47. Frontal gait disorder Also called gait apraxia where there is loss of ability to use legs properly in walking w/o demonstrable sensory impairment, weakness, or incoordination . Usually occurs in frontal lobe lesion ,NPH, Binswanger disease, Pick’s disease. It is characterized by slightly flexed posture, short, shuffling steps and an inability to integrate and coordinate lower extremity movement to accomplish normal ambulation.

48. Normal pressure Hydrocephalus

49. 76 year old female came with C/O forgetfullness , difficulty in remembering names , decreased fluency had trouble in performing learned motor skills with difficulty in initiating gait (GAIT APRAXIA) On examination there was decline in memory and orientation with no sensory or motor weakness.MRI and CT scan showing predominant cortical and hippocampal atrophy.

50. ALZHEIMER DISEASE RISK Factors : Old age / female sex / low level of education / diabetes Mutations in gene encoding presinilin1 and presinilin 2 Characterised by memory impairment –difficulty in naming , Aphasia is early and prominent feature . Normal results on lab MRI shows predominant hippocampal atrophy

51. Steppage gait Weakness of dorsiflexor - Tibialis anterior , The steps are regular and even, but the advancing foot hangs with the toes pointing toward the ground . high steppage gait in order to help the foot clear the floor and avoid tripping. Double tap Causes: u/l foot drop - peroneal nerve palsy, L5 radiculopathy . polio, Multiple Sclerosis , GBS, Spinal disc herniation peroneal muscle atrophy, Peroneal nerve injury polyneuropathy

52. Waddling / Trendelenburg gait During stance phase of gait cycle centre of gravity is tranferred to the stance leg . Hip abducters stabilizes the pelvis. Abducter weakness of the stance leg causes downward tilt of opposite pelvis to reduce the load by deceasing the lever arm The patient walks with a broad base,with an exaggerated rotation of pelvis that results in a waddling gait. . Causes-proximal muscle weakness, cushings , polymyositis dermatomyosiitis ,LGMD,CDH, MND